Cancer immune evasion through KRAS and PD-L1 and potential therapeutic interventions.


Journal

Cell communication and signaling : CCS
ISSN: 1478-811X
Titre abrégé: Cell Commun Signal
Pays: England
ID NLM: 101170464

Informations de publication

Date de publication:
02 03 2023
Historique:
received: 01 11 2022
accepted: 31 01 2023
entrez: 2 3 2023
pubmed: 3 3 2023
medline: 7 3 2023
Statut: epublish

Résumé

Oncogenic driver mutations have implications that extend beyond cancer cells themselves. Aberrant tumour cell signalling has various effects on the tumour microenvironment and anti-tumour immunity, with important consequences for therapy response and resistance. We provide an overview of how mutant RAS, one of the most prevalent oncogenic drivers in cancer, can instigate immune evasion programs at the tumour cell level and through remodelling interactions with the innate and adaptive immune cell compartments. Finally, we describe how immune evasion networks focused on RAS, and the immune checkpoint molecule PD-L1 can be disrupted through therapeutic intervention, and discuss potential strategies for combinatorial treatment. Video abstract.

Identifiants

pubmed: 36864508
doi: 10.1186/s12964-023-01063-x
pii: 10.1186/s12964-023-01063-x
pmc: PMC9979509
doi:

Substances chimiques

B7-H1 Antigen 0
Proto-Oncogene Proteins p21(ras) EC 3.6.5.2
KRAS protein, human 0

Types de publication

Video-Audio Media Journal Article Review Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

45

Subventions

Organisme : Wellcome Trust
Pays : United Kingdom
Organisme : Wellcome Trust
ID : 206194
Pays : United Kingdom

Informations de copyright

© 2023. The Author(s).

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Auteurs

Alex Watterson (A)

Translational Cancer Genomics, Wellcome Sanger Institute, Hinxton, UK.
Open Targets, Cambridge, UK.

Matthew A Coelho (MA)

Translational Cancer Genomics, Wellcome Sanger Institute, Hinxton, UK. matthew.coelho@sanger.ac.uk.
Open Targets, Cambridge, UK. matthew.coelho@sanger.ac.uk.

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